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Immunity. 2014 Oct 16;41(4):518-28. doi: 10.1016/j.immuni.2014.09.008.

HIF transcription factors, inflammation, and immunity.

Author information

1
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
2
Division of Biology, University of California, San Diego, La Jolla, CA 92093, USA.
3
Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093, USA; Glycobiology Research and Training Center, University of California, San Diego, La Jolla, CA 92093, USA.
4
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK; Department of Cell and Molecular Biology, Karolinska Institute, 171 77 Stockholm, Sweden. Electronic address: rsj33@cam.ac.uk.

Abstract

The hypoxic response in cells and tissues is mediated by the family of hypoxia-inducible factor (HIF) transcription factors; these play an integral role in the metabolic changes that drive cellular adaptation to low oxygen availability. HIF expression and stabilization in immune cells can be triggered by hypoxia, but also by other factors associated with pathological stress: e.g., inflammation, infectious microorganisms, and cancer. HIF induces a number of aspects of host immune function, from boosting phagocyte microbicidal capacity to driving T cell differentiation and cytotoxic activity. Cellular metabolism is emerging as a key regulator of immunity, and it constitutes another layer of fine-tuned immune control by HIF that can dictate myeloid cell and lymphocyte development, fate, and function. Here we discuss how oxygen sensing in the immune microenvironment shapes immunological response and examine how HIF and the hypoxia pathway control innate and adaptive immunity.

PMID:
25367569
PMCID:
PMC4346319
DOI:
10.1016/j.immuni.2014.09.008
[Indexed for MEDLINE]
Free PMC Article

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